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PHPY 302 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

What are the four parts of an electrocardiogram and what do they mean?

A

P wave is the depolarization of the atria
QRS complex is the depolarization of the ventricles
T wave is the repolarization of the ventricles
U wave is not completely know but is likely the repolarization of the papillary muscle

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2
Q

What is isovolumic ventricular contraction?

A

This begins with the closure of the mitral valve (generates the first heart sound). The blood volume is the end-diastolic volume and the ventricles are beginning to contract

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3
Q

What is ventricular ejection?

A

This begins with the opening of the semilunar valve due to an increase in ventricular pressure. The blood is ejected from the ventricle. This ends with the closure of the semilunar valve

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4
Q

What is isovolumic ventricular relaxation?

A

This begins with the closure of the semilunar valve (2nd heart sound). The blood volume in the ventricle is the end-systolic volume. The ventricle is relaxing

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5
Q

What is ventricular filling?

A

This begins with the opening of the mitral valve due to the low ventricular pressure. Passive filling occurs and is followed by active filling due to the contraction of the atria

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6
Q

What is the ventricular pressure volume loop?

A

A plot which is generated by plotting ventricular pressure against ventricular volume. It showcases the dynamic changes during one cardiac cycle

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7
Q

What is the equation for cardiac output?

A

CO = HR x SV

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8
Q

What is stroke volume?

A

The amount of blood pumped out of the ventricle per beat

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9
Q

What is cardiac output?

A

The output of the heart per unit time

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10
Q

What is cardiac index?

A

The cardiac output per body surface area. This is used to minimize the influence of body size on cardiac output

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11
Q

What impact does increasing heart rate have on stroke volume and cardiac output?

A

Increasing the heart rate will decrease the stroke volume and increase the cardiac output (to a point, eventually cardiac output will decrease)

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12
Q

Why does exercising cause CO and HR to increase so much?

A

Reduction of peripheral vascular resistance, positive inotropic effect to the contractile myocytes by an increase in sympathetic activity, and compressing action of the skeletal muscles with the venous valves to enhance venous return

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13
Q

How do you calculate stroke volume?

A

SV= EDV - ESV

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14
Q

What can impact stroke volume?

A

Preload, afterload, and contracitilty

HR can have an effect also, but it is much smaller

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15
Q

How does preload impact SV?

A

Increasing preload will increase SV

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16
Q

What impacts preload?

A

The degree of stretching of cardiac myocytes prior to contraction

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17
Q

What is the formula for compliance?

A

Change in volume/ Change in pressure

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18
Q

What do high and low compliance mean?

A

High compliance means the heart can be easily stretched during diastole
Low compliance means the heart will resist expansion during diastole

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19
Q

How does compliance relate to end-diastolic pressure-volume relationship?

A

It is the inverse of the slope

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20
Q

How does ventricular dilation impact EDV and EDP?

A

There is an increase in ventricular compliance so the ventricle can have an increased EDV without a large impact on the EDP

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21
Q

How does ventricular hypertrophy impact EDV and EDP?

A

There is a decrease in ventricular compliance with causes an increase in the EDP for a given EDV

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22
Q

What does an increase in venous return cause?

A

An increase in ventricular filling, so an increase in preload. This will increase EDP for a given heart.

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23
Q

What does the Frank-Starling mechanism explain?

A

The phenomena through which an increase in preload creates and increase in the force of contraction of the heart

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24
Q

What is the purpose of the Frank-Starling mechanism?

A

To ensure the outputs of both ventricles are matched so there is no shift in blood between the pulmonary and systemic circulations

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25
Q

What will an increase in venous return cause with respect to ESV?

A

The SV and CO will increase, but there will be no change in the ESV

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26
Q

What happens if an increase in SV due to an increase in VR changes the contractility status of the heart?

A

A decrease in ESV would occur

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27
Q

What is the length-tension relationship of the ventricle?

A

The relationship between changes of the initial length of a myocyte to the contractile force developed by the heart muscle

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28
Q

What does increasing the preload do to the force?

A

Increasing the preload increases the tension developed, which increases the velocity of tension development, and increases the force

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29
Q

What is the afterload?

A

The ventricular wall tension developed during ventricular ejection.

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30
Q

Ventricular wall stress can be estimated using what?

A

Laplace’s law for a sphere

Wall stress = (Intraventricular pressure x preload)/2(Wall thickness)

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31
Q

How is ventricular hypertrophy an adaptive mechanism?

A

To offset the increase in wall sress

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32
Q

What occurs in congestiv eheart failure?

A

The Frank-Starling mechanism fails to compensate for the increase in preload due to the decrease in contractile function

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33
Q

How does an increase in afterload impact the pressure needed?

A

A much higher pressure is needed to eject the same volume of blood

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34
Q

How does an increase in afterload impact SV?

A

Decreases the velocity of fibre shortening which results in a decrease in SV

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35
Q

What is the Y-intercept of a force-velocity relationship curve?

A

The maximum velocity that can be achieved by the muscle fiber in the absence of any load

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36
Q

What is the X-intercept of a force-relationship velocity curve?

A

The maximum force that the heart can generate at a given preload condition

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37
Q

How do changes in afterload impact preload?

A

When afterload increases the ventricle has to generate higher pressure to open the aortic valve. This decreases ejection velocity and increases ESV. This will cause an increase in EDV, and a decrease in SV.

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38
Q

What is contractility?

A

The property of contractile myocytes that account for the strength of contraction

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39
Q

How can ventricular EDP be used to evaluate cardiac performance?

A

Inadequate systolic emptying will increase ESV, which will increase EDV, which will increase EDP

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40
Q

How does stroke volume change in relation to a hearts contractility when EDV and EDP are increased?

A

The heart with the stronger contractility will have a larger increase in stroke volume

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41
Q

How does an increase in preload effect the stroke volume of a failing heart?

A

It has minimal impact because a failing heart already has a much higher EDP at a given stroke volume

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42
Q

In the case of ventricular hypertrophy, what does a small increase in EDV cause?

A

A large increase in EDP due to the low ventricular compliance of the heart

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43
Q

How does an increase in contractility impact cardiac index?

A

An increase in contractility increases SV and in turn generates a higher cardiac index

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44
Q

How can stroke volume be used to measure cardiac performace?

A

The higher the SV at a given preload that shorter the fiber lengths and smaller the ventricular chamber size.

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45
Q

What is the ejection fraction?

A

The fraction of the EDV ejected from the ventricle during each systolic contraction

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46
Q

What is the equation for ejection fraction?

A

EF = SV/EDV

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47
Q

When is ventricular pressure usually the highest?

A

Just before the opening of the semilunar valves

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48
Q

What is the Treppe phenomenon (Bowditch effect)?

A

Increase in heart rate reduces the time for Na-K ATPase to restore the concentration gradient which increases the amount of sodium in the cytosolic space. This inhibits Na-Ca exchanger activities and increases the Ca in the cytosolic space. This causes an increase in myocardial contractility

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49
Q

How will an increase in intropy impact the ESPVR?

A

ESPVR will move upward and to the left. It will also have a steeper slope

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50
Q

What is the best indicator of contractility?

A

Vmax

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51
Q

How will Vmax change if contractility is increased?

A

It will cause a parallel shift up and to the right

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52
Q

What is aortic stenosis?

A

Narrow opening of the aortic valve

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53
Q

What does the increase velocity of blood associated with aortic stenosis cause?

A

Turbulent flow which generates a systolic murmur

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54
Q

What does aortic stenosis cause in respect to cardiac output?

A

An increase in LVP, which causes and increase in afterload, which causes an increase in ESV and a decrease in stroke volume and cardiac output

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55
Q

What is mitral stenosis?

A

Improper opening of the mitral valve

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56
Q

What does resistance to flow due to mitral stenosis cause in the atrium?

A

Elevation of left atrial pressure

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57
Q

What contributes to incomplete ventricular fillinf?

A

Elevation of left atrial pressure (retention of blood in the atrium) and a decrease in EDV due to reduced venous return

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58
Q

What do the higher velocities of blood flow cause in mitral stenosis?

A

A diastolic murmur between S2 and S1

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59
Q

What is aortic insufficiency?

A

Incomplete closure of the aortic valve which allows for movement of blood between the aorta and the left ventricle at all times

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60
Q

How is stroke volume impacted by aortic insufficiency?

A

Preload increases which increases the peak systolic pressure. EDV and EDP are also increased which augment the increase in force of contraction which leads to an increase in SV.

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61
Q

What causes a diastolic murmur to be heard with aortic insufficiency?

A

Regurgitation during ventricular diastole

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62
Q

What is mitral insufficiency?

A

Incomplete closure of the mitral valve. This allows blood flow between the atrium and the ventricle constantly

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63
Q

What causes a systolic murmur in mitral insufficiency?

A

The back flow of blood during ventricular systole

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64
Q

What causes the rise in LAP during ventricular systole with mitral insufficiency?

A

Regurgitation of blood from the ventricle back to the atrium

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65
Q

How do EDV and ESV change with mitral insufficiency and why?

A

EDV is increased due to the increase in LV filling with the increase in LAP
ESV decreases because blood from the ventricle is regurgitated back to the LA during systole

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66
Q

What is physiological ventricular hypertrophy (Concentric hypertrophy)?

A

An adapting change to stress in order to enhance pumping capacity of the heart
This is reversible and non-pathological

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67
Q

What is afterload related pathological ventricular hypertrophy?

A

Induced by chronic increase in afterload, so the ventricle needs to generate a greater pressure chronically to eject the blood

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68
Q

What can afterload related pathological ventricular hypertrophy lead to?

A

Reduction in SV and elevation in ESP

Can cause diastolic dysfunction and heart failure

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69
Q

What is preload related pathological ventricular hypertrophy (eccentric hypertrophy)?

A

An increase in ventricular wall stress caused by volume overload. This causes systolic dysfunction

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70
Q

What does preload related pathological ventricular hypertrophy cause?

A

A huge increase in ESV and EDV with minimal changes in EDP due to the high compliance. SV is decreased

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71
Q

What are the two pacemakers and what are their rates?

A

Sinoatrial node which beats at around 70-80 BPM

The atrioventricular node which beats at around 40-60 BPM

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72
Q

What are pacemaker cells responsible for?

A

The genesis of automaticity leading to cardiac muscle contraction

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73
Q

What is autorhythmicity?

A

The combination of both the automaticity and rhythmicity properties. Automaticity is the ability of the cell to initiate its own pacemaking
Rhythmicity is the ability of a cell to maintain the regularity of pacemaking activity

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74
Q

In the ionic basis of automaticity what is phase 4?

A

It is initiated by the slow leak of Na and followed by Ca influx

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75
Q

In the ionic basis of automaticity what is phase 0?

A

It is the depolarization with calcium influx through the long-lasting voltage-gated channels after reaching threshold

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76
Q

In the ionic basis of automaticity what is phase 3?

A

Repolarization accomplished by rapid potassium efflux

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77
Q

What are the three variables that can influence cardiac rhythmicity?

A

Rate of diastolic depolarization, maximum diastolic potential, and threshold potential

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78
Q

What are the three regions of the AV node and how do they impact ventricular filling?

A

Atrionodal region, nodal region, and nodal-His
The atrionodal and nodal regions are the principle delay between atrial and ventricular contraction. This ensures ventricular filling

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79
Q

Where is the atrioventricular bundle and where does it go?

A

Located below the AV node and passes through the fibrous ring that separates the atria and the ventricles. It reaches the inter-ventricular septum to form two separated branches

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80
Q

Where are the bundle branches and how to they impact the depolarization?

A

A continuation of the AV bundle which is divided into left and right. The right bundle is considerably longer and thinner than the left bundle branch, which allows for septal depolarization from left to right

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81
Q

What are the Purkinje fibers and what is their job?

A

Inferior terminal branches of the bundle branches which have the fastest rate of conduction. They enable rapid, organized, and near synchronous depolarization and contraction of the ventricles

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82
Q

What are James fibers?

A

Fibers from the atrial inter-nodal tracts that pass around the AV node and enter the inter-ventricular septum.

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83
Q

What problems are associated with James fibers?

A

Pre-excitation can occur, which means the signals are not coming from the AV node and there is no delay for ventricular filling

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84
Q

What is paroxysmal?

A

The sudden onset of rapid or abnormal rhythms

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85
Q

What are Mahaim fibers?

A

Any direct connections between AV node, bundle of His, or bundle branches into the interventricular septum

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86
Q

What is the bundle of Kent?

A

A muscular bundle forming a direct connection between atrial and ventricular myocardium

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87
Q

What is the bundle of Kent capable of doing?

A

It can take the action potential back to the atrium, so one signal from the SA node can cause two heart beats

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88
Q

What is an electrocardiogram?

A

A graphic recording of the biopotentials generated by the myocardium during the cardiac cycle

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89
Q

How do the lengths of systole and diastole compare in a regular cardiac cycle?

A

Systole is shorter than diastole

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90
Q

What is the paper speed, square time, and square amplitude in a regular ECG?

A

The paper speed is 25mm/sec so each square is 0.04 seconds. One square of amplitude is equal to 0.1mV

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91
Q

What is the PR interval?

A

From the start of atrial depolarization (P wave) to the start of ventricular depolarization (R wave)
The time required for the depolarization wave from the SA node to spread through the right atrium and the duration of atrial contraction

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92
Q

What is the PR segment?

A

The end of atrial depolarization (P wave) to the start of ventricular depolarization (R wave)
This is the length of time of delay for the action potential passing through the AV node

93
Q

What is the QRS duration?

A

From the beginning of the Q wave to the end of the S wave. This is the duration of ventricular depolarization.

94
Q

What is the ST segment?

A

The end of ventricular depolarization (S wave) to the beginning of ventricular repolarization (T wave)
This is also known as the isoelectric line and it should be flat

95
Q

What is the QT interval?

A

The beginning of ventricular depolarization (Q wave) to the end of ventricular repolarization (T wave)
This is the duration of ventricular action potentials and is correlated with heart rate

96
Q

What is indicated by an abnormal PR interval?

A

A short PR interval could indicate Wolff-Parkinson-White Syndrome
A long PR interval could indicate a heart block

97
Q

What is indicated by an abnormal QRS complex?

A

A wide QRS complex could mean a bundle branch block

A tall QRS complex could mean ventricular hypertrophy

98
Q

What is indicated by an abnormal ST segment?

A

Elevation could indicate epicardial ischemia

Depression could indicate endocardial ischemia

99
Q

What is indicated by an abnormal T wave?

A

An inverted T wave could indicate myocardial ischemia, intraventricular conduction delay, or an anxiety attack

100
Q

Which limbs of an ECG are bipolar and which are unipolar?

A

Leads 1-3 are bipolar

Leads aVR, aVL, aVF, and V1-V6 are unipolar

101
Q

Where do the bipolar leads connect?

A

Lead one has the negative at the right arm and the positive at the left arm
Lead two has the negative at the right arm and the positive at the left leg
Lead three has the negative at the left arm and the positive at the left leg

102
Q

What is overdrive suppression?

A

Pacemaker cells with higher intrinsic rhythm prevent all latent pacemakers in the heart from firing

103
Q

How does heart tissue become hyperpolarized and what can this cause?

A

Heart cells become more negative from the Na-K ATPase pump working. This means it takes a longer time for the current to reach threshold, so automaticity is slowed.

104
Q

What is the phenomenon of the re-entry loop?

A

Cardiac impulses may re-excite the myocytes through which it had passed previously within the same cardiac cycle

105
Q

What are the three conditions required for re-entry to occur?

A

Closed conduction loop, unidirectional block, and sufficiently slow conduction around the loop

106
Q

What is a sinus rhythm?

A

SA node controls the cardiac rhythm

107
Q

What is sinus bradycardia?

A

Sinus rhythm with a rate less than 60 BPM

108
Q

What is sinus tachycardia?

A

Sinus rhythm with a greater than 100 BPM

109
Q

What is arrythmia?

A

Onset of abnormal heart rhythms

110
Q

What is escape rhythm?

A

Prolonged impairment of SA node allows latent pacemaker to initiate an escape beat

111
Q

What is an escape rhythm?

A

A situation when SA node has a lower automaticity than that of the AV node

112
Q

What is an ectopic beat?

A

Any heart beat generated by impulse other than the one from SA node

113
Q

Why does the impulse from latent pacemakers travel in two directions?

A

The AV node is in between the atrium and ventricles. An impulse travels towards the ventricles and towards the atrium, which leads to an inverted P wave

114
Q

What is a ventricular escape rhythm?

A

Conduction blockage of the AV allows bundle of His or bundle branches to become latent pacemaker

115
Q

What is ventricular tachycardia?

A

High heart rate (usually over 120) with a wide QRS complex

116
Q

What is ventricular flutter?

A

A very high heart rate (over 200BPM) but a lowered cardiac output

117
Q

What is ventricular fibrillation?

A

Nonfunctional muscle contraction (quivering) which produces 0 cardiac output

118
Q

What is heart block?

A

Impaired conduction through the AV conduction system

119
Q

What is a first-degree AV block?

A

There is an increased delay between atrial and ventricular depolarization. The PR interval is longer

120
Q

What is a Mobitz 1 second-degree AV block?

A

The PR interval progressively lengthens until a QRS complex is absent. After the absence it continues to repeat.

121
Q

What is the Mobitz 2 second-degree block?

A

There is no gradual lengthening of PR intervals, but occasionally QRS complexes will disappear

122
Q

What is a third degree AV block?

A

Complete heart block with complete failure of conduction between the atria and ventricles

123
Q

What occurs if there is a right bundle branch block?

A

There is normal conduction down the left bundle branch and the right ventricle is depolarized via gap junctions

124
Q

What occurs if there is a left bundle branch block?

A

Occurs when transmission of impulses does not reach the left ventricle. The left ventricle is depolarized via gap junctions

125
Q

What is hemodynamics?

A

The study of the fluid mechanics of blood

126
Q

What is the A wave of atrial pressure?

A

The rising phase occurs due to atrial systole after the rapid ventricular filling phase

127
Q

What is the C wave of atrial pressure?

A

The closure of the tricuspid valve while atrial filling continues

128
Q

What is the region between the a and c waves in atrial filling?

A

The end of active ventricular filling (atrial relaxation)

129
Q

What is the V wave of atrial pressure?

A

The filling of the atrium after it is fully stretched

130
Q

What is pulmonary wedge pressure used for?

A

To estimate atrial pressure

131
Q

What do you use to measure pulmonary wedge pressure?

A

Swan-Ganz catheter

132
Q

What causes changes in blood velocity?

A

The diameter of the vessel

133
Q

Which region of the cardiovascular system has the largest cross sectional area?

A

The capillaries

134
Q

What is hydraulic resistance?

A

The changes in pressure divided by flow rate

135
Q

What is the dominant factor in determining resistance to flow?

A

The radius of the vessels

136
Q

How are the branches of the vascular system arranged?

A

Parallel to eachother

137
Q

What is the primary resistance vessel?

A

Arterioles

138
Q

What innervates the resistance vessels?

A

Autonomic nerves

139
Q

What is used to predict the flow pattern?

A

Reynolds number

Re=pQD/uA

140
Q

What does a flow pattern less than 2000 or more than 3000 mean?

A

Less than 2000 means laminar flow and more than 3000 means turbulent flow

141
Q

What is the flow rate proportional to in laminar flow?

A

Pressure drop

142
Q

What is flow rate proportional to in turbulent flow?

A

The square root of pressure drop

143
Q

What is hematocrit?

A

The ratio of volume of red blood cells to volume of whole blood

144
Q

Why do arteries have a tendency to collapse?

A

Due to the elastic property of the elastic and collagen fibers enclosing the artery
Due to active tension by vascular smooth muscle cells

145
Q

What is the critical closing pressure for a given blood vessel?

A

The mean blood pressure at or below which the blood vessel will collapse

146
Q

What is the effective circulating volume?

A

The blood volume within the vasculature that can be utilized to perfuse the organ systems within our body

147
Q

What is blood pressure?

A

The force exerted by blood against a vessel wall

148
Q

What is peripheral vascular resistance?

A

The diameter of the small arteries and arterioles which contributes to the resistance to flow between the arterial and venous compartments

149
Q

What is the equation for systemic vascular resistance?

A

SVR= (MAP- CVP)/CO
MAP is mean arterial pressure
CVP is central venous pressure

150
Q

What is systolic pressure?

A

The upper limit of the periodic oscillations of blood pressure initiated by the ventricular systole
Usually around 120mmHg

151
Q

What is diastolic pressure?

A

The minimum pressure within the arteries during ventricular diastole
Usually around 80mmHg

152
Q

What is pulse pressure?

A

The difference between systolic and diastolic pressure

153
Q

What is mean arterial pressure?

A

The average pressure in the arteries over time

Calculated by 1/3 SP + 2/3 DP

154
Q

What are high pressure baroreceptors?

A

The primary sensors for the detection of arterial blood pressure changes

155
Q

Where are high pressure baroreceptors located?

A

The carotid sinus and the aortic arch

156
Q

What impact do high pressure baroreceptors have?

A

They are stretch receptors that when fired cause inhibitory sympathetic effects and excitatory parasympathetic effects to result in lowered blood pressure and heart rate

157
Q

Where are low pressure baroreceptors located?

A

Venoatrial junctions, cardiopulmonary, and low pressure chambers of the heart

158
Q

What do type A fibers of atrial baroreceptors do?

A

Fire during atrial depolarization to monitor heart rate

159
Q

What do type B fibers of atrial baroreceptors do?

A

Fire during ventricular systole for the monitoring of atrial volume

160
Q

What does the bainbridge refelx do?

A

Increase in stretching of the B fibers increases HR when baseline HR is low. This acts as a counterbalance to the high pressure baroreceptors when increase firing of the high pressure baroreceptors causes a decrease in HR

161
Q

What do chemoreceptors detect?

A

Changes in PO2, PCO2, and H concentrations

162
Q

What is the primary function of chemoreceptors?

A

To regulate respiratory activity and to maintain the blood gas level within a narrow physiological range

163
Q

What can cardiovascular function be controlled by?

A

Blood pressure and blood volume

164
Q

What are the two categories of cardiovascular function control?

A

Neural and humoral

165
Q

What are the three levels of neural control of cardiovascular function?

A

Cortex, hypothalamus, and the medulla

166
Q

What is the cortex responsible for in neural control of cardiovascular function?

A

Altering cardiovascular function during emotional stress

167
Q

What is the hypothalamus responsible for in neural control of cardiovascular function?

A

Modulating medullary neuronal activity

168
Q

Why is the resting heart rate lower than the intrinsic firing rate of the SA node?

A

Parasympathetic nuclei are tonically active

169
Q

What does vagal stimulation causing the release of acetylcholine cause?

A

Negative chronotropy, dromotropy, and inotropy

170
Q

Where are the negative inotropic effects due to parasympathetic innervation more evident?

A

The atria

171
Q

Where do the right and left vagus nerves innervate during parasympathetic innervation?

A

The right innervates the SA node

The left innervates the AV node and the ventricular conduction systems

172
Q

What does stimulation of sympathetic innervation do to cardiovascular function?

A

Causes tachycardia and vasoconstriction

173
Q

What does sympathetic innervation and norepinephrine release cause?

A

Increase in chronotropy, dromotropy, and inotropy

174
Q

What causes transient coronary vasoconstriction?

A

Sympathetic stimulation of the heart

175
Q

What is the primary variable that needs to be regulated to control cardiovascular function?

A

Systemic arterial blood pressure

176
Q

Where do catecholamines come from and what activates their release?

A

The adrenal medulla

Activated by the preganglionic sympathetic nerves during times of stress

177
Q

What occurs humorally when epinephrine is present in low levels?

A

Vasodilation due to the greater affinity for B2 receptors

178
Q

What occurs humorally when epinephrine is present in low to moderate levels?

A

Increase in heart rate, contractility, and conduction velocity

179
Q

What are the three basic mechanisms by which epinephrine increases blood pressure?

A

Direct stimulation of myocytes in ventricles, increase in heart rate, and vasoconstriction in resistance vessels and veins

180
Q

What is norepinephrine an agonist of?

A

B1 and a

181
Q

What does norepinephrine cause in the heart?

A

Increase in systolic and diastolic pressure. Increase in peripheral resistance
Increase and then decrease in HR

182
Q

What is epinephrine an agonist of?

A

B1, B2, and a

183
Q

What does epinephrine increase in the heart?

A

HR, CO, and SV due to B1 activation

184
Q

What is isoproterenol an agonist of?

A

Non-specific B agonist

185
Q

What occurs humorally when epinephrine is present in high levels?

A

Increase in cardiac output and systemic vascular resistance

186
Q

What does the renin-angiotensin-aldosterone system cause?

A

Increased blood pressure and blood volume

187
Q

What does the atrial natriuretic peptide cause?

A

Decreased blood pressure and volume

188
Q

What does vasopressin cause?

A

Increase in blood pressure and blood volume

189
Q

What is ventricular end diastolic volume a function of?

A

Ventricular filling pressure, ventricular filling time, and ventricular compliance

190
Q

How will an increase in the rate of output impact atrial pressure?

A

Right atrial pressure will decrease

If flow continues to increase, pressure will drop to a negative value

191
Q

What causes the plateau phase in the vascular function curve?

A

The negative right atrial pressure

192
Q

What happens when cardiac output is zero?

A

The veins are closing. This is the mean systemic filing pressure, which is also the closing pressure

193
Q

What is mean systemic filling pressure a function of?

A

Fluid volume (directly) and overall compliance (inversely)

194
Q

What is central venous pressure?

A

The blood pressure in the thoracic vena cava in the proximity of the right atrium

195
Q

What is the equation for venous compliance?

A

C=V/P
C is Compliance
V is change in blood volume
P is change in CVP

196
Q

What does the vascular function curve describe?

A

The relationship between CVP and CO

197
Q

How does transfusion impact CVP?

A

It increases, because blood volume is higher

198
Q

How does hemorrhage impact CVP?

A

It lowers it, because blood volume is lower

199
Q

How does vasodilation impact CVP?

A

It increases it, because venous blood volume increases due to decreased resistance

200
Q

How does vasoconstriction impact CVP?

A

It lowers it, because venous blood volume decreases due to increased resistance

201
Q

How does increasing sympathetic stimulation impact CVP?

A

It will decrease due to the increase in CO

202
Q

How does increasing peripheral resistance impact CO and CVP?

A

CVP remains relatively unchanged (lowered volume and constricted vessels counterbalance)
CO decreases

203
Q

How does heart failure impact CO and CVP?

A

CO decreases so CVP increases

204
Q

How does hypervolemia impact CO and CVP?

A

CO increases due to increased preload

CVP increases due to increased blood volume

205
Q

How much of the body weight is blood?

A

7-8%

206
Q

How much of the blood volume is cellular component?

A

Around 45%

207
Q

How much more numerous are erythrocytes than white blood cells and platelets?

A

700x more than WBC

17x more than platelets

208
Q

What is the bone marrow broken up to produce and in which ratios?

A

25% red blood cells and 75% white blood cells

209
Q

Why is the concentration of red blood cells so much higher than that of white blood cells in the blood?

A

White blood cells often have a shorter life span and they undergo transendothelial migration, leaving the blood

210
Q

How much of the plasma is water?

A

92%

211
Q

What are the major plasma proteins?

A

Albumins, fibrinogen, globulins, and coagulation factors

212
Q

What is hemostasis?

A

Arrest of bleeding or prevention of hemorrhage

213
Q

What occurs in the vascular phase of hemostasis?

A

Contraction of vascular smooth muscle cells within the damaged vessel

214
Q

What happens neurally during the vascular phase of hemostasis?

A

Increase in sympathetic tone to cause vasoconstriction

215
Q

What happens chemically during the vascular phase of hemostasis?

A

Chemical byproducts of activated platelets and coagulation promotes vasoconstriction

216
Q

What occurs during platelet adhesion?

A

Platelets bind to themselves or to other components

217
Q

What occurs during platelet activation?

A

Platelets undergo exocytosis of their storage granules. This causes amplification of the platelet activation response

218
Q

What occurs during platelet aggregation?

A

They form molecular bridges between platelets and subendothelial structures such as collagen and fibrinogen

219
Q

What is the end result of platelet adhesion, activation, and aggregation?

A

The formation of a platelet plug

220
Q

What is coagulation?

A

The process of blood clot formation

221
Q

What are blood clots made of?

A

Mesh of fibrin containing blood cells and serum

222
Q

What activates the intrinsic pathway of coagulation?

A

Tissue factors released by the damaged tissue

223
Q

What activates the intrinsic pathway of coagulation?

A

Factor 12 coming in contact with damaged blood vessels

224
Q

What is necessary for coagulation?

A

A functional liver and vitamin K

225
Q

What is fibrinolysis?

A

Degradation of fibrin which holds together the blood clot

226
Q

What does tissue plasminogen activator do?

A

It is an enzyme produced by damaged endothelial cells which catalyzes the conversion of plasminogen into plasmin

227
Q

What is streptokinase?

A

A product of the beta hemolytic streptococcus that can be used as a fibrinolytic agent

228
Q

What is urokinase?

A

A protease expressed by the plasminogen activator urokinase gene that is involved in degradation of the extracellular matrix

PHPY 302 (4 decks)

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